Rheumatoid Arthritis (RA) is characterized by synovial inflammation and destruction of joint cartilage and bone. Such destruction is caused in part by the ongoing synthesis of proinflammatory cytokines and matrix metalloproteinases. Autoimmune diseases, such as RA have been classically viewed as Th1 (CD4+ T helper cell-induced; interferon-gamma, for example, is produced, which activates the bactericidal activities of macrophages and induces B-cells to make opsonizing (coating) antibodies, leading to cellular immunity) and not Th2 (CD4+ T helper cell-induced; interleukin 4, for example, is released, which results in the activation of B-cells to make neutralizing antibodies, leading to humoral immunity) disorders. However, recent studies have brought this thought into questions (Lubberts; Seminars in Immunopathology 32(1), 43-53 (2010)). For example, IL-17a (a proinflammatory cytokine) is present at sufficient concentrations in the sinovial fluid of RA patient joints that it can be detected. However, this and other cytokines cannot be detected in serum or plasma obtained from the same patients. There is a need to detect biomarkers in serum or plasma that are related to RA and other inflammatory disorders (e.g., Crohn's Disease, Inflammatory Bowel Disease (IBD), ulcerative colitis, psoriasis, Chronic Obstructive Pulmonary Disease (COPD)) so that RA can be more readily or effectively diagnosed and staged, risk for developing RA or other inflammatory disorder can be more readily or effectively assessed, and patients who are responders and non-responders to RA therapy can be more readily or effectively identified.